2. Accountability is another key to success. Consider documenting your program and progress on a free website such as FitDay, SparkPeople, 3FatChicks, Calorie Count (http://caloriecount.about.com), or others. Consider blogging about your weight-loss adventure on a free platform such as WordPress or Blogger. Such a public commitment may be just what you need to keep you motivated.

3. Do you have a friend or spouse who wants to lose weight? Start the same program at the same time and support each other. That’s built-in accountability.

4. If you tend to over-eat, floss and brush your teeth after you’re full. You’ll be less likely to go back for more anytime soon.

5. Eat at least two or three meals daily. Skipping meals may lead to uncontrollable overeating later on. On the other hand, ignore the diet gurus who say you must eat every two or three hours. That’s codswallop.

6. Eat meals at a leisurely pace, chewing and enjoying each bite thoroughly before swallowing.

7. Plan to give yourself a specific reward for every 10 pounds (4.5 kg) of weight lost. You know what you like. Consider a weekend get-away, a trip to the beauty salon, jewelry, an evening at the theater, a professional massage, home entertainment equip-ment, new clothes, etc.

8. Carefully consider when would be a good time to start your new lifestyle. It should be a period of low or usual stress. Bad times would be Thanksgiving day, Christmas/New Years’ holiday, the first day of a Caribbean cruise, and during a divorce.

Christmas holiday isn’t the best time to start a diet. New Years’ Day is better.

9. If you know you’ve eaten enough at a meal to satisfy your nutritional requirements yet you still feel hungry, drink a large glass of water and wait a while.

10. Limit television to a maximum of a few hours a day.

11. Maintain a consistent eating pattern throughout the week and year.

12. Eat breakfast routinely.

13. Control emotional eating.

14. Weigh frequently: daily during active weight-loss efforts and during the first two months of your maintenance-of-weight-loss phase. After that, cut back to weekly weights if you want. Daily weights will remind you how hard you worked to achieve your goal.

15. Be aware that you might regain five or 10 pounds (2-4 kg) of fat now and then. You probably will. Don’t freak out. It’s human nature. You’re not a failure; you’re human. But draw the line and get back on the old weight-loss program for one or two months. Analyze and learn from the episode. Why did it happen? Slipping back into your old ways? Slacking off on exercise? Too many special occasion feasts or cheat days? Allowing junk food back into the house?

16. Learn which food item is your nemesis—the food that consistently torpedoes your resolve to eat right. For example, mine is anything sweet. Remember an old ad campaign for a potato chip: “Betcha can’t eat just one!”? Well, I can’t eat just one cookie. So I don’t get started. I might eat one if it’s the last one available. Or I satisfy my sweet craving with a diet soda, small piece of dark chocolate, or sugar-free gelatin. Just as a recovering alcoholic can’t drink any alcohol, perhaps you should totally abstain from…? You know your own personal gastronomic Achilles heel. Or heels. Experiment with various strategies for vanquishing your nemesis.

My nemesis

17. If you’re not losing excess weight as expected (about a pound or half a kilogram per week), you may benefit from eating just two meals a day. This will often turn on your cellular weight-loss machinery even when total calorie consumption doesn’t seem much less than usual. The two meals to eat would be breakfast and a mid-afternoon meal (call it what you wish). The key is to not eat within six hours of bedtime. Of course, this trick could cause dangerous hypoglycemia if you’re taking drugs with potential to cause low blood sugars, like insulin and sulfonylureas. Talk to your dietitian or physician before instituting a semi-radical diet change like this.

18. One of the bloggers I followed when I had time is James Fell. He says, “If you want to lose weight you need to cook. Period.” James blogs at http://www.sixpackabs.com, with a focus on exercise and fitness.

19. Regular exercise is much more important for prevention of weight regain rather than for actually losing weight.

James P. Grantham and Maciej Henneberg of the School of Medical Sciences (University of Adelaide, Adelaide, Australia) suggest that estrogen-like compounds in the environment are causing obesity. Read about their hypothesis in a recent issue of PLOS One. I don’t know if they’re right, but their idea deserves consideration.

A panel of university-based scientists convened by The Endocrine Society recently reviewed the available literature on health effects of endocrine-disrupting chemicals (aka EDCs). The executive summary is available free online. Some excerpts:

The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information.

* * *

Both cellular and animal models demonstrate a role for EDCs in the etiology of obesity and T2D [type 2 diabetes]. For obesity, animal studies show that EDC-induced weight gain depends on the timing of exposure and the age of the animals. Exposures during the perinatal period [the weeks before and after birth] trigger obesity later in life. New results covering a whole range of EDC doses have underscored the importance of nonmonotonic dose-response relationships; some doses induced weight increase, whereas others did not. Furthermore, EDCs elicit obesity by acting directly on white adipose tissue, al- though brain, liver, and even the endocrine pancreas may be direct targets as well.

Regarding T2D, animal studies indicate that some EDCs directly target 􏰁beta and alpha cells in the pancreas, adipocytes, and liver cells and provoke insulin resistance together with hyperinsulinemia. These changes can also be associated with altered levels of adiponectin and leptin— often in the absence of weight gain. This diabetogenic action is also a risk factor for cardiovascular diseases, and hyperinsulinemia can drive diet-induced obesity. Epide- miological studies in humans also point to an association between EDC exposures and obesity and/or T2D; however, because many epidemiological studies are cross-sectional, with diet as an important confounding factor in humans, it is not yet possible to infer causality.

Dr. Sinha practices internal medicine in northern California (Silicon Valley) and has a large dose of South Asians in his clinic. “South Asia” usually encompasses India, Pakistan, Nepal, Bangladesh, Bhutan, Sri Lanka and Maldives. It is home to one fifth of the world’s population. This book pertains mostly to Indians, which is Dr. Sinha’s ethnicity. I live in the Pheonix, AZ, area and we have a fair number of Indian engineers and physicians.

WHY DO SOUTH ASIANS NEED THEIR OWN SPECIAL HEALTH GUIDE?

Because Dr. Sinha says they have unique genetic and cultural issues that predispose them to type 2 diabetes, abdominal obesity, coronary artery disease, high blood pressure, and adverse cholesterol numbers. For example, compared to natives who stay in their home countries, South Asian immigrants to the West have 3–4 times higher prevalence of diabetes, he says. Dr Sinha has a program that he’s convinced will prevent or forestall these medical problems in South Asians.

Dr. Sinha says South Asians eat too many carbohydrates and are too sedentary. Especially those who have moved to the West (e.g., US, UK, Europe, Canada). He notes that the core of the typical South Asian diet is flat breads, lentils, rice, fried crispy snacks (with heart-poisoning trans fats), culminating in 150–200 daily grams of carbohydrate more than he sees in other ethnics in California. Western fast foods, sodas, and sweets compound the problem.

He says “most South Asians are skinny-fat,” meaning skinny legs and arms but with a fat belly from visceral fat. This is also called sarcopenic obesity. The usual “healthy” body mass index (BMI) numbers don’t apply to Asians. The World Health Organisation classifies Asians as underweight if BMI is 18.4 or less, healthy at BMI of 18.5 to 13, overweight at BMI 23.1 to 25, and obese if BMi is over 25. These numbers are lower than those used for non-Asian populations.

Another issue in his South Asian patient population is vitamin D deficiency related to their dark skin (hence, less vitamin D production) and too much time indoors. He says vitamin D deficiency promotes inflammation and insulin resistance. More on this below.

Some South Asians have a K121Q gene mutation that causes insulin resistance, which in turn can cause disease. And whether it’s genetic or not (but I think it is), he says South Asians tend to have higher Lp(a) [aka lipoprotein(a)], which causes early and aggressive coronary artery disease. They also tend to have small dense LDL, leading to a lower-than-expected total cholesterol level which may be deceptively low.

Sinha notes a strong vegetarian preference in Indians but spends almost no time discussing it. From the book, I can’t tell if Indian vegetarians are lacto-ovo-vegetarians, pescetarians, or vegans. The author is not a vegetarian.

Gadi Sagar temple on Gadisar Lake, Jaisalmer, Rajasthan, India

SINHA’S GRAND UNIFICATION THEORY OF DISEASE CAUSATION

So, South Asians, at least in the West, have a high-carb diet, are too sedentary, and have genetic tendencies to heart disease and diabetes. How do these factors cause disease? It’s all tied together with insulin resistance. Insulin is the main hormone that keeps our blood sugar from rising too high after we digest a meal. Insulin drives blood sugar into our body cells to be used as energy or stored as fat or glycogen. If our tissues have insulin resistance, blood sugar levels rise. As a compensatory effort, our pancreas excretes more insulin in to the blood stream than would normally be the case. Whether or not that eventually lowers blood sugar levels, the higher insulin levels themselves can cause toxicity. For example, higher insulin levels raise blood pressure, which damages the cells lining the insides of our arteries, leading to chronic inflammation and atherosclerosis (hardening of the arteries). Some of the arterial damage is mediated through small dense LDL cholesterols (aka type B LDL), which is promoted by high insulin levels (hyperinsulinemia). Insulin resistance also results in a defective and overactive immune system, which further promotes chronic inflammation. This inflammation is “…the root cause of almost every imaginable chronic disease…from heart attacks and strokes to Alzheimers Disease.”

Anyway, this is Dr. Sinha’s hypothesis, and there is some scientific evidence to support it. Sinha says that the concept of insulin resistance “weaves together virtually every chronic ailment currently afflicting South Asians.” That may be a bit hyperbolic: He carves out no exceptions for arthritis, asthma, eczema, migraines, glaucoma, macular degeneration, hearing loss, erectile dysfunction, hepatitis C, prostate enlargement, toenail fungus, or male-pattern baldness.

Dr. Sinha’s Grand Unification Theory of Disease Causation has some support among physicians and scientists, but is by no means universally accepted among them. As for myself, I think he’s over-simplifying (for his readership’s sake?) and getting a bit ahead of the science.

Most clinicians aren’t testing directly for insulin resistance. What are the indirect clues? Belly fat, low HDL cholesterol, high trigylcerides, high blood pressure, prediabetes, and type 2 diabetes. These are components of the metabolic syndrome. Not everybody with one or more of these factors has insulin resistance but many do.

WHAT’S HIS PROGRAM?

If Sinha is correct, the South Asian Health Solution is a “low-insulin lifestyle” achieved through carbohydrate-reduced eating, exercise, and avoidance or resolution of belly fat. These help improve all components of the aforementioned metabolic syndrome. The backbone of the plan is carbohydrate restriction. For low-carb eating, avoid wheat bread and Indian flat breads (e.g., chapatis, naans, parathas, puris, phulkas), aloo (primarily potatoes and starchy vegetables), rice and other grains, beans, and sugar. Keep track of your net carbohydrates (he likes FitnessPal.com, which includes South Asian foods).

If you need to burn off body fat, limit carbs to 50–100 grams/day (digestible or net carbs, I assume). Aim for 100–150 grams/day to maintain health and weight loss.

Dr. Sinha doesn’t provide a comprehensive meal plan. He trusts his California South Asians to figure out how and what to eat. They’re smarter than average (he never says that, but that’s been my experience with South Asians in my world).

Dr. Sinha is also a huge proponent of exercise. He’ll tell you about squats, lunges, planks, burpees, yoga, and Tabata intervals. He agrees with me and Franziska Spritzler that “physical activity is the most effective fountain of youth available.”

Taking a rest from the fountain of youth

I skipped some of the chapters due to lack of time and interest: women’s issues (e.g., pregnancy, polycystic ovary syndrome, post-partum depression, osteoporosis), childhood, fatigue and stress management, and anti-aging.

Non-alcoholic steatohepatitis (NASH) is quite common in South Asians, seemingly linked to visceral (abdominal) obesity and insulin resistance related to carbohydrates.

The book has no specific focus on diabetes.

THUMBS UP OR DOWN?

Overall, I like many of Dr. Sinha’s ideas. They seem to be supported by his experience with his own patients. I trust him. I bet many South Asians and non-Asians eating the Standard American Diet would see improved health by following his low-carb, physically active program.

Investigators affiliated with universities in Italy and Greece wondered about the effect on obesity of two ketogenic “Mediterranean” diet spells interspersed with a traditional Mediterranean diet over the course of one year. They found significant weight loss, and perhaps more importantly, noregain of lost weight over the year, on average.

This was a retrospective review of medical records of patients of a private nutritional service in three fitness and weight control centers in Italy between 2006 and 2010. It’s unclear whether patients were paying for fitness/weight loss services. 327 patient records were examined. Of these, 89 obese participants met the inclusion and exclusion criteria and started the program; 68 completed it and were the ones analyzed. (That’s not at all a bad drop-out rate for a year-long study.) The completers were 59 males and 12 females (I know, the numbers don’t add up, but that’s what they reported). Ages were between 25 and 65. Average weight was 101 kg (222 lb), average BMI 35.8, average age 49. All were Caucasian. No diabetics.

Here’s the program:

20 days of a very-low-carb ketogenic diet, then

20 days of a low-carbohydrate non-ketogenic diet for stabilization, then

4 months of a normal caloric Mediterranean diet, then

repeat #1 and #2, then

6 months of a normal caloric Mediterranean diet

In the ketogenic phases, which the authors referred to as KEMEPHY, participants followed a commercially available protocol called TISANOREICA. KEMEPHY is combination of four herbal extracts that is ill-defined (at least in this article), with the idea of ameliorating weakness and tiredness during ketosis. The investigators called this a ketogenic Mediterranean diet, although I saw little “Mediterranean” about it. They ate “beef & veal, poultry, fish, raw and cooked green vegetables without restriction, cold cuts (dried beef, carpaccio and cured ham), eggs and seasoned cheese (e.g., parmesan).” Coffee and tea were allowed. Items to avoid included alcohol, bread, pasta, rice, milk, and yogurt. “In addition to facilitate the adhesion to the nutritional regime, each subject was given a variety of specialty meals constituted principally of protein and fibers. “These meals (TISANOREICA) that are composed of a protein blend obtained from soya, peas, oats (equivalent to 18 g/portion) and virtually zero carbohydrate (but that mimic their taste) were included in the standard ration.” They took a multivitamin every morning. Prescribed carbohydrate was about 30 grams a day, with macronutrient distribution of 12% carb, 36 or 41% protein, and 51 0r 52% fat. It appears that prescribed daily calories averaged 976 (but how can that be prescribed when some food items are “unrestricted”?).

After the first and second active weight loss ketogenic phases, participants ate what sounds like a traditional Mediterranean diet. Average prescribed macronutrient distribution was 57% carbohydrate, 15 % protein, and 27% fat. Wine was allowed. It looks like 1800 calories a day were recommended.

Food consumption was measured via analysis of 3-day diaries, but you have to guess how often that was done because the authors don’t say. The results of the diary analyses are not reported.

What Did They Find?

Most of the weight loss occurred during the two ketogenic phases. Average weight loss in the first ketogenic period was 7.4 kg (16 lb), and another 5.2 kg (11 lb) in the second ketogenic period. Overall average weight loss for the entire year was 16.1 kg (35 lb).

Average systolic blood pressure over the year dropped a statistically significant 8 units over the year, from 125 to 116 mmHg.

Over the 12 months, they found stable and statistically significant drops in total cholesterol, LDL cholesterol (“bad cholesterol”), triglycerides, and blood sugar levels. No change in HDL cholesterol (“good cholesterol”).

Liver and kidney function tests didn’t change.

The authors didn’t give explanations for the drop-outs.

Although the group on average didn’t regain lost weight, eight participants regained most of it. The investigators write that “…the post dietary analysis showed that they were not compliant with nutritional guidelines given for the Mediterranean diet period. These subjects returned to their previous nutrition habits (“junk” food, high glycaemic index, etc.) with a mean “real” daily intake of 2470 Kcal rather than the prescribed 1800 Kcal.”

Comments

A key take-home point for me is that the traditional Mediterranean diet prevented the weight regain that we see with many, if not most, successful diets.

However, most formulas for calculating steady state caloric requirements would suggest these guys would burn more than the 1800 daily calories recommended to them during the “normal calorie” months. How hard did the dieters work to keep calories around 1800? We can only speculate.

Although the researchers describe the long periods of traditional Mediterranean diet as “normal caloric,” they don’t say how that calorie level was determined and achieved in the real world. Trust me, you can get fat eating the Mediterranean diet if you eat too much.

I’ll be the first to admit a variety of weight loss diets work, at least short-term. The problem is that people go back to their old ways of eating regain much of the lost weight, typically starting six months after starting the program. It was smart for the investigators to place that second ketogenic phase just before the typical regain would have started!

There are so few women in this study that it would be impossible to generalize results to women. Why so few? Furthermore, weight loss and other results weren’t broken down for each sex.

I suspect the results of this study will be used for marketing KEMEPHY and TISANOREICA. For all I know, that’s why the study was done. We’re trusting the investigators to have done a fair job choosing which patient charts to analyze retrospectively. They could have cherry-picked only the good ones. Some of the funding was from universities, some was from Gianluca Mech SpA (what’s that?).

How much of the success of this protocol is due to the herbal extracts and TISANOREICA? I have no idea.

The authors made no mention of the fact the average fasting glucose at baseline was 103 mg/dl (5.7 mmol/l). That’s elevated into the prediabetic range. So probably half of these folks had prediabetes. After the one-year program, average fasting glucose was normal at 95 mg/dl (5.3 mmol/l).

The improved lipids, blood sugars, and lower blood pressure may have simply reflected successful weight loss and therefore could have been achieved by a variety of diets.

The authors attribute their success to the weight-losing metabolic effects of the ketogenic diet (particularly the relatively high protein content), combined with the traditional Mediterranean diet preventing weight regain.

The authors write:

The Mediterranean diet is associated with a longer life span, lower rates of coronary heart disease, hypercholesterolemia, hypertension, diabetes and obesity. But it is difficult to isolate the “healthy” constituents of the Mediterranean diet, since it is not a single entity and varies between regions and countries. All things considered there is no “one size fits all” dietary recommendation and for this reason we have tried to merge the benefits of these two approaches: the long term “all-life” Mediterranean diet coupled with brief periods of a metabolism enhancing ketogenic diet.

Salmon is one the the cold-water fatty fish loaded with healthful omega-3 fatty acids, but also persistent organic pollutants

It sounds like Jerome Ruzzin is convinced that’s the case. I put some thought into it last August and was skeptical—still am, but I’m keeping an open mind. Mr. Ruzzin has a review article published in 2012 at BMC Public Health (“Public health concern behind the exposure to persistent organic pollutants and the risk of metabolic diseases”). Here’s his summary:

The global prevalence of metabolic diseases like obesity and type 2 diabetes, and its colossal economic and social costs represent a major public health issue for our societies. There is now solid evidence demonstrating the contribution of POPs [persistent organic pollutants], at environmental levels, to metabolic disorders. Thus, human exposure to POPs might have, for decades, been sufficient and enough to participate to the epidemics of obesity and type 2 diabetes. Based on recent studies, the fundaments of current risk assessment of POPs, like “concept of additive effects” or “dioxins and dl-PCBs induced similar biological effects through AhR”, appear unlikely to predict the risk of metabolic diseases. Furthermore, POP regulation in food products should be harmonized and re-evaluated to better protect consumers. Neglecting the novel and emerging knowledge about the link between POPs and metabolic diseases will have significant health impacts for the general population and the next generations.

Medical student Kris Gunnars has an article at Business Insider, of all places, that shows graphically many of the major U.S. dietary changes of the last hundred years. In this case, transmogrification may be a better term than mere “changes.” Much of the Western world has evolved in similar fashion.

You need to read the article and ponder the graphs if you question why we have so much obesity, type 2 diabetes, heart disease, hypertension, and perhaps cancer. You’ll see dramatic increases in consumption of added sugars, industrial seed oils (esp. soybean), soda pop and fruit juice (added sugar!), total calories, and fast food. You’ll see how much we’ve increased dining away from home. Butter consumption is down drastically, but doesn’t seem to have done us much good, if any.

Sugar cane

There’s fairly good evidence that coronary artery disease (CAD) the cause of most heart attacks) was very prominent between 1960 to 2000 or so, but it’s been tapering off in recent years and didn’t seem to be very common 100 years ago. Understand that you can have it for 20 years or more before you ever have symptoms (angina) or a heart attack from it. In fact, the disease probably starts in childhood. I’ve always wondered about the cause of the CAD prevalence trends, and wondered specifically how much of the long-term trend was related to trans-fat consumption. But I’ve never been able to find good data on trans-fat consumption. Kris came up with a chart of margarine consumption, which may be a good proxy for trans-fats. Another of his charts includes shortening, a rich source of trans-fats and probably also a good proxy. I remember growing up in the 1960s that we always had a 1/2 gallon tin can of Crisco hydrogenated fat in the cupboard. Shortening consumption increased dramatically from 1955 until dropping like a rock around 2000.

The timeline curves for trans-fat consumption (by proxy) and prevalence of coronary heart disease seem to match up fairly well, considering a 20 year lag. In the early 1990s, we started cutting back on trans-fats, and here we are now with lower mortality and morbidity from coronary artery disease. (CAD is very complex; lower rates of smoking surely explain some of the recent trend.)

Links

“Do not be deceived: God cannot be mocked. A man reaps what he sows. Whoever sows to please their flesh, from the flesh will reap destruction; whoever sows to please the Spirit, from the Spirit will reap eternal life.”